Is Fructose Linked to Adiposity in Babies? (FLAB)

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The fetal fractional thigh volume will me measured in addition to routine fetal measurements at 32 weeks estimated gestation age. This measurement is a measure of neonatal adiposity.

Current Other Outcome Measures

Not Provided

Original Other Outcome Measures

Not Provided

Descriptive Information

Brief Title

Is Fructose Linked to Adiposity in Babies?

Official Title

Is Fructose Linked to Adiposity in Babies?

Brief Summary

The obesity epidemic has reached down into the infant and toddler age group. Dietary indiscretion during pregnancy, particularly in our current food environment, is a major risk factor for both gestational diabetes and neonatal macrosomia (>4kg newborns), which is itself a risk factor for obesity and metabolic syndrome in the offspring, possibly even during childhood. Temporal increases in fructose consumption in the last two decades coincide with temporal increases weight gain during pregnancy and with increased birth weight, including a higher prevalence of macrosomic newborns. Our central hypothesis is that higher fructose consumption during pregnancy is a risk factor for infant obesity and metabolic syndrome.

Detailed Description

The "fetal origins hypothesis" suggests that an individual's risk for obesity and metabolic disorders begins in utero; that fetal or early postnatal exposure to environmental factors, such as maternal nutrition or endocrine disrupting chemicals, adversely influences early development and results in permanent changes affecting energy storage and expenditure.

Most studies on "fetal origins" of obesity in the offspring have focused on maternal high-fat diets; yet dietary fat consumption has not changed appreciably in the last two decades. One chemical exposure in both pregnant mothers and newborns that has been steadily increasing worldwide is fructose. Although ostensibly a carbohydrate, fructose is a potent lipogenic substrate, and in the hypercaloric state, as much as 30% of an ingested fructose load undergoes de novo lipogenesis to form triglyceride thus the effects of high-fat and high-fructose diets in terms of physiology and outcome are comparable. Substituting sucrose (fructose + glucose) for glucose alone increases visceral adiposity, insulin resistance, and dyslipidemia in adult animals and humans. For humans, fructose is ubiquitous in the food environment, especially for pregnant mothers, who are often counseled to drink juice during pregnancy, as it is deemed to be healthier than soda. The effects of fructose consumption during pregnancy on infant birth weight and adiposity has not yet been studied.

Study Type

Observational

Study Design

Observational Model: CohortTime Perspective: Prospective

Target Follow-Up Duration

Not Provided

Biospecimen

Not Provided

Sampling Method

Non-Probability Sample

Study Population

Pregnant women between 18 to 40 years of age are eligible for this study

Condition

Obesity

Metabolic Syndrome

Intervention

Not Provided

Study Groups/Cohorts

Not Provided

Publications *

Not Provided

* Includes publications given by the data provider as well as publications
identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.

Recruitment Information

Recruitment Status

Completed

Enrollment

40

Completion Date

January 2013

Primary Completion Date

June 2012 (Final data collection date for primary outcome measure)

Eligibility Criteria

Inclusion Criteria:

Agreement to participate in all measurements

Plans to remain in the area through delivery

Ability to understand and give informed consent in either English or Spanish.

Exclusion Criteria:

Presence of diabetes prior to the index pregnancy

Presence of gestational diabetes during a previous pregnancy

Presence of diabetes or of other chronic metabolic disease such as cardiovascular disease, active thyroid disease, liver disease, pulmonary or psychiatric disorders, HIV

Any disorder requiring diet therapy (i.e., renal insufficiency)

Multiple gestation

Prior history of intrauterine growth retardation

Use of substances known to cause intrauterine growth retardation (e.g., smoking or drug use). -

Once recruited, any ultrasonographic evidence of intrauterine growth retardation during the course of the pregnancy would also lead to exclusion.

Sex/Gender

Sexes Eligible for Study:

Female

Ages

18 Years to 40 Years (Adult)

Accepts Healthy Volunteers

Yes

Contacts

Contact information is only displayed when the study is recruiting subjects